This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. This research goal was to uncover the physiological relevance of an acidic motif that occurs within the N-terminal domain of an invertebrate accessory beta subunit of voltage-gated calcium channels . Specifically, this acidic motif dampens the amplitude of the calcium current. This suppressive effect is more pronounced in the presence of intracellular NaCl or Mg-ATP, but not in the presence of non-chelated ATP, suggesting that the function of the acidic motif is sensitive to the ionic composition of the intracellular solution. From January to May (2008) I started exploring the relationships between the structure and function of this acidic motif. To this end, I generated several deletion mutants of this beta subunit that differ in the length of the acidic motif. Mutants lacking a few acidic residues of the motif still have a significant effect in dampening the calcium current, whereas mutants lacking a significant portion of the acidic motif have relatively low influence on the amplitude of the calcium current. At UPenn, this work continues exploring the relationships between structure, function and physiology of the acidic motif of this calcium channel beta subunit expressed by Schistosoma mansoni, using biochemical and electrophysiological approaches. Hopefully, these studies will contribute to the understanding of the biology and physiology of this human pathogen.